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First, the hyperacetylation of the mitochondrial malate-aspartate shuttle protein inhibits the oxidation and transport of NADH in the mitochondria, resulting in an imbalance of redox in the cytoplasm

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Dose-related increases in resting heart rate have also been reported in clinical studies

This is in stark contrast to their differential responses to the natural stimulus diacetyl (Fig 4B and C)

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